{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Kozela E"],"funding":["Dr. Miriam and Sheldon G. Adelson Medical Research Foundation","NINDS NIH HHS","NINDS Informatics Center for Neurogenetics and Neurogenomics"],"pagination":["136"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4891926"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13(1)"],"pubmed_abstract":["<h4>Background</h4>Our previous studies showed that the non-psychoactive cannabinoid, cannabidiol (CBD), ameliorates the clinical symptoms in mouse myelin oligodendrocyte glycoprotein (MOG)35-55-induced experimental autoimmune encephalomyelitis model of multiple sclerosis (MS) as well as decreases the memory MOG35-55-specific T cell (TMOG) proliferation and cytokine secretion including IL-17, a key autoimmune factor. The mechanisms of these activities are currently poorly understood.<h4>Methods</h4>Herein, using microarray-based gene expression profiling, we describe gene networks and intracellular pathways involved in CBD-induced suppression of these activated memory TMOG cells. Encephalitogenic TMOG cells were stimulated with MOG35-55 in the presence of spleen-derived antigen presenting "],"journal":["Journal of neuroinflammation"],"pubmed_title":["Pathways and gene networks mediating the regulatory effects of cannabidiol, a nonpsychoactive cannabinoid, in autoimmune T cells."],"pmcid":["PMC4891926"],"funding_grant_id":["P30 NS062691"],"pubmed_authors":["Juknat A","Vogel Z","Kozela E","Kaushansky N","Gao F","Coppola G"],"additional_accession":[]},"is_claimable":false,"name":"Pathways and gene networks mediating the regulatory effects of cannabidiol, a nonpsychoactive cannabinoid, in autoimmune T cells.","description":"<h4>Background</h4>Our previous studies showed that the non-psychoactive cannabinoid, cannabidiol (CBD), ameliorates the clinical symptoms in mouse myelin oligodendrocyte glycoprotein (MOG)35-55-induced experimental autoimmune encephalomyelitis model of multiple sclerosis (MS) as well as decreases the memory MOG35-55-specific T cell (TMOG) proliferation and cytokine secretion including IL-17, a key autoimmune factor. The mechanisms of these activities are currently poorly understood.<h4>Methods</h4>Herein, using microarray-based gene expression profiling, we describe gene networks and intracellular pathways involved in CBD-induced suppression of these activated memory TMOG cells. Encephalitogenic TMOG cells were stimulated with MOG35-55 in the presence of spleen-derived antigen presenting ","dates":{"release":"2016-01-01T00:00:00Z","publication":"2016 Jun","modification":"2026-06-14T09:51:41.965Z","creation":"2019-03-27T02:15:15Z"},"accession":"S-EPMC4891926","cross_references":{"pubmed":["27256343"],"doi":["10.1186/s12974-016-0603-x"]}}